Düsing R, Moritz J, Glänzer K, Kramer H J
Br J Clin Pharmacol. 1985 Jan;19(1):29-35. doi: 10.1111/j.1365-2125.1985.tb02609.x.
The effects of nonpressor doses of intravenous angiotensin II and of the converting enzyme inhibitor captopril on renal excretory function were investigated in eight healthy volunteers during sustained water diuresis on a constant intake of 150 mmol sodium per day. The angiotensin II-analogue val5-angiotensin II-asp1-beta-amide was infused i.v. at an average dose of 2.6 ng kg-1 min-1 which was the highest dose without a significant effect on arterial blood pressure. This subpressor dose of angiotensin II significantly decreased urine volume, urinary excretion of sodium, chloride and phosphate and distal delivery [(CH2O + CCl)/GFR X 100] in the absence of changes in GFR or distal fractional chloride absorption [CH2O/(CH2O + CCl)]. In a second series of experiments, an oral dose of 50 mg of the angiotensin I-converting enzyme inhibitor captopril was given to the sodium replete volunteers. In this study, captopril did not affect arterial blood pressure, GFR or any of the determined parameters of renal tubular function. Our results strongly suggest that the nonpressor dose of angiotensin II induced renal retention of sodium chloride via increased absorption in the proximal tubule. Thus, they further support the concept that angiotensin II participates in the regulation of renal sodium chloride excretion by affecting proximal tubular absorptive capacity. However, in the sodium replete stage, angiotensin II is of no major importance in regulating sodium chloride excretion.
在8名健康志愿者中进行了研究，这些志愿者每日持续摄入150 mmol钠，处于持续水利尿状态，以探究静脉注射非升压剂量的血管紧张素II和转换酶抑制剂卡托普利对肾脏排泄功能的影响。静脉输注血管紧张素II类似物缬氨酸5 - 血管紧张素II - 天冬酰胺1 - β - 酰胺，平均剂量为2.6 ng·kg⁻¹·min⁻¹，此为对动脉血压无显著影响的最高剂量。这种血管紧张素II的亚升压剂量显著降低了尿量、钠、氯和磷酸盐的尿排泄量以及远端输送量[（CH₂O + CCl）/GFR×100]，而肾小球滤过率（GFR）或远端氯分数吸收[CH₂O/（CH₂O + CCl）]无变化。在第二系列实验中，给钠储备充足的志愿者口服50 mg血管紧张素I转换酶抑制剂卡托普利。在本研究中，卡托普利未影响动脉血压、GFR或任何测定的肾小管功能参数。我们的结果强烈表明，血管紧张素II的非升压剂量通过增加近端小管的吸收导致肾脏对氯化钠的潴留。因此，它们进一步支持了血管紧张素II通过影响近端小管吸收能力参与肾脏氯化钠排泄调节的概念。然而，在钠储备充足阶段，血管紧张素II在调节氯化钠排泄方面并非至关重要。
